ArticleNature2017
Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 151 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
151 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.
- MYT1L: A systematic review of genetic variation encompassing schizophrenia and autism.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2020Pooled it
- FFPE-CUTAC: A Single Assay, Multiple Layers.bioRxiv : the preprint server for biology · 2026Article
- The SynMuvA lin-15A licenses natural transdifferentiation by antagonizing identity safeguarding mechanisms.PLoS genetics · 2026Article
- Deep molecular profiling of lung neuroendocrine tumours and supra-carcinoids.Molecular cancer · 2026Article
- Distinct media requirements for dopaminergic neuron reprogramming from human glia and fibroblasts.Scientific reports · 2026Article
- APOBEC2 deficiency disrupts hematopoietic lineage commitment, resulting in emergence of dual identity lymphocytes in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Aberrant chromatin remodeling influences human neural cell fate change in Trisomy 21.bioRxiv : the preprint server for biology · 2026Article
- Decoding sequence determinants of gene expression in diverse cellular and disease states.Nature methods · 2026Article
- Combinatorial transcription factor interactions drive modular gene regulatory networks.bioRxiv : the preprint server for biology · 2026Article
- Multi-omics profiling reveals MAGEL2-driven defects in human corticogenesis shared across Prader-Willi and Schaaf-Yang syndromes.bioRxiv : the preprint server for biology · 2026Article
- The DNA Demethylase TET1 is a Pivotal Regulator of the miR-124/ISX9-Instructed Conversion of Astrocytes to Induced Neurons.Molecular neurobiology · 2026Article
- Redefining cellular reprogramming with advanced genomic technologies.Nature reviews. Genetics · 2026Review
- Pbx1 and Pbx3 cooperatively regulate intermediate progenitor genesis and corticogenesis in the mouse neocortex.Frontiers in cell and developmental biology · 2026Article
- The Mechanisms and Application Prospects of Astrocyte Reprogramming into Neurons in Central Nervous System Diseases.Current neuropharmacology · 2026Review
- ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis.Nature communications · 2025Article
- KMT2D temporally activates neuronal transcriptional factor genes to mediate cerebellar granule cell differentiation.Science advances · 2025Article
- A survey of hypothalamic phenotypes identifies molecular and behavioral consequences of MYT1L haploinsufficiency in male and female mice.Hormones and behavior · 2025Article
- Direct transdifferentiation of tumorigenic melanoma cells induces tumor cell reversion.Cell death & disease · 2025Article
- From Adipose to Action: Reprogramming Stem Cells for Functional Neural Progenitors for Neural Regenerative Therapy.International journal of molecular sciences · 2025Review
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
91 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
Abstract
Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.